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103 UNDERSTANDING PATHOPHYSIOLOGY OF HYPERVENTILATION IN CIRRHOSIS SJ Varghese1, KV Kuppu Rao2, J Randhir1, A Murali1, V Jayanthi1, S Sowmya2 INTRODUCTION: Hyperventilation which is an effect of hypoxia has been well documented in hepatic cirrhosis. Hypoxia in cirrhosis could be due to intrapulmonary vasodilatation/shunt (IPVS), defective diffusion capacity (DLCO < 80%), increased alveolar arterial oxygen gradient {(A-a)O2 > 15 mm of Hg} and mechanical causes such as pleural effusion, ascites, etc. Hyperventilation may also be due to respiratory centre stimulation by certain substances which are otherwise metabolized by the normal liver.
1Department of Medical Gastroenterology, Stanley Medical College Hospital; 2Tuberculosis Research Centre, Chetpet, Chennai, India
AIM: To find out the relationship between hyperventilation with IPVS, (A-a)O2, DLCO and substances such as progesterone and lactic acid.
METHODS: Out of one hundred cirrhotic patients registered in the liver clinic, thirty three patients were nonsmoking men without pulmonary diseases and ascites were included in this study. All underwent transcutaneous 2D contrast echocardiography, pulmonary function tests, arterial blood gas analysis, oxygen dissociation curve plotting and estimation of blood progesterone and lactic acid.
RESULTS: Thirty three cirrhotic men with a mean age of 41.84 ± 11.4 years. Out of them, 6 and 27 belonged to Child's A and B respectively. Etiology of cirrhosis was ethanol in 18 patients, viral in 8 and others in 8 men. Out of 33 patients, 29 (87.87%) had abnormal DCLO, 17 (51.51%) had elevated (A-a)O2, 19 (57.57%) had IPVD. The mean PaCO2 was 28.27 ± 7.6, 28.74 ± 5.6 & 31.53 ± 5.9 respectively and which indicated hyperventilation resulting in respiratory alkalosis. Mean value of P50 of the oxygen dissociation curve was 25.41 ± 1.1, 25.24 ± 0.7 and 25.28 ± 1.0 respectively ie, there was a left sided shift which also confirms alkalosis respectively. Four patients (13.79%) had mild hypoxemia (PaO2 60 to 80 mm of Hg); one (3.3%) had severe hypoxemia (PaO2 < 60 mm of Hg) and the rest (82.9%) had normal PaO2. The lactic acid & progesterone were elevated in 13 (39.39%) & 16 (48.48%) patients respectively.
CONCLUSION: Hyperventilation was the effect of either defective diffusion capacity or elevated (A-a)O2 or presence of IPVD or presence of elevated progesterone, lactic acid in the blood or a combination which tries to keep PaO2 in the normal range.